Objective To determine whether preoperative anthropometric and computed tomography (CT) measurements of body composition can predict postoperative morbidity and mortality in patients with gastric or esophageal cancer. Materials and Methods This was a retrospective study in which we reviewed the medical records and abdominal CT scans of patients with gastric or esophageal cancer who underwent surgery in 2015 at a cancer center. CT scans performed during routine preoperative evaluation were retrospectively assessed to measure the area of lean body mass at the level of the third lumbar vertebra, as well as the area of visceral and subcutaneous fat. Results Seventy patients were included in the study. The mean age was 59.9 years (range, 33-82 years), and 47 patients (67.1%) were men. The mean postoperative follow-up period was 14.9 months. Neither postoperative morbidity nor postoperative mortality correlated significantly with gender, age, the type of primary tumor, the presence of comorbidities, smoking status, body mass index, nutritional status, or visceral fat area. The survival rate was higher for patients with normal lean body mass than for those with low lean body mass (hazard ratio = 0.116; 95% confidence interval 0.015-0.906; p = 0.040). Conclusion Our data suggest that lean body mass can be a relevant prognostic factor in patients with gastric or esophageal cancer, and that CT measurements should be included in the routine preoperative evaluation, because it may provide information that aids nutritional and clinical care for these patients.The development of left ventricular thrombus (LVT) is a well-known and serious complication of acute myocardial infarction (AMI) due to the risk of systemic arterial embolism (SE), which is variable in its clinical picture and has potentially serious consequences depending on the extent of target organ damage. SE results in an increase in mortality and morbidity in these patients. LVT is one of the main causes of the development of ischaemic cardio-embolic cardiovascular events (CVE) after MI and the determination of the source of cardiac embolus is crucial for the initiation of adequate anticoagulant therapy in secondary prevention. Echocardiography holds an irreplaceable place in the diagnosis of LVT, contrast enhancement provides higher sensitivity. The gold standard for LVT diagnosis is cardiac magnetic resonance imaging, but it is not suitable as a basic screening test. In patients with already diagnosed LVT, it is necessary to adjust antithrombotic therapy by starting warfarin anticoagulation for at least 6 months with the need for echocardiographic follow-up to detect thrombotic residues. The effect of prophylactic administration of warfarin in high-risk patients after anterior AMI does not outweigh the risk of severe bleeding complications and does not result in a decrease in mortality and morbidity. At the present time, there is not enough evidence to use direct oral anticoagulants in this indication.An amendment to this paper has been published and can be accessed via a link at the top of the paper.An amendment to this paper has been published and can be accessed via a link at the top of the paper.An amendment to this paper has been published and can be accessed via a link at the top of the paper.BACKGROUND Perturbation of the major UGT2B17-dependent androgen catabolism pathway has the potential to affect prostate cancer (PCa) progression. The objective was to evaluate UGT2B17 protein expression in primary tumours in relation to hormone levels, disease characteristics and cancer evolution. METHODS We conducted an analysis of a high-density prostate tumour tissue microarray consisting of 239 localised PCa cases treated by radical prostatectomy (RP). Cox proportional hazard ratio analysis was used to evaluate biochemical recurrence (BCR), and a linear regression model evaluated variations in circulating hormone levels measured by mass spectrometry. The transcriptome of UGT2B17 in PCa was established by using RNA-sequencing data. RESULTS UGT2B17 expression in primary tumours was associated with node-positive disease at RP and linked to circulating levels of 3α-diol-17 glucuronide, a major circulating DHT metabolite produced by the UGT2B17 pathway. UGT2B17 was an independent prognostic factor linked to BCR after RP, and its overexpression was associated with development of metastasis. Finally, we demonstrated that distinctive alternative promoters dictate UGT2B17-dependent androgen catabolism in localised and metastatic PCa. CONCLUSIONS The androgen-inactivating gene UGT2B17 is controlled by overlooked regulatory regions in PCa. UGT2B17 expression in primary tumours influences the steroidome, and is associated with relevant clinical outcomes, such as BCR and metastasis.The best-known role of UDP-glucuronosyltransferase enzymes (UGTs) in cancer is the metabolic inactivation of drug therapies. By conjugating glucuronic acid to lipophilic drugs, UGTs impair the biological activity and enhance the water solubility of these agents, driving their elimination. Multiple clinical observations support an expanding role for UGTs as modulators of the drug response and in mediating drug resistance in numerous cancer types. However, accumulating evidence also suggests an influence of the UGT pathway on cancer progression. Dysregulation of the&nbsp;expression and activity of UGTs has been associated with the progression of several cancers, arguing for UGTs as possible mediators of oncogenic pathways and/or disease accelerators in a drug-naive context. https://www.selleckchem.com/products/azd5153-6-hydroxy-2-naphthoic-acid.html The consequences of altered UGT activity on tumour biology are incompletely understood. They might be associated with perturbed levels of bioactive endogenous metabolites such as steroids and bioactive lipids that are inactivated by UGTs or through non-enzymatic mechanisms, thereby eliciting oncogenic signalling cascades. This review highlights the evidence supporting dual roles for the UGT pathway, affecting cancer progression and drug resistance. Pharmacogenomic testing of UGT profiles in patients and the development of therapeutic options that impair UGT actions could provide useful prognostic and predictive biomarkers and enhance the efficacy of anti-cancer drugs.